Chapter 20
the heart
Anatomy review
Electrical activity of the whole heart (EKG)
Electrical activity of the heart cells
The Cardiac Cycle
Cardiac Input and Output (dynamics)
Heart review
4 chambers
2 atria
2 ventricles
receive
send
4 valves
2 AV valves
2 semilunar valves
2 circuits
systemic
pulmonary
external heart anatomy
fig. 20-9
internal heart anatomy
fig. 20-6
100 keys (pg. 678)
“The heart has four chambers, two associated
with the pulmonary circuit (right atrium and right
ventricle) and two with the systemic circuit (left
atria and left ventricle). The left ventricle has a
greater workload and is much more massive
than the right ventricle, but the two chambers
pump equal amounts of blood. AV valves
prevent backflow from the ventricles into the
atria, and semilunar valves prevent backflow
from the aortic and pulmonary trunks into the
ventricles.”
cardiac conduction system
modified cardiac muscle cells
•SA node (sinoatrial node)
wall of RA
•AV node (atrioventricular node)
between atrium and ventricle
•conducting cells
AV bundle (of His)
conducting fibers
Purkinje fibers
conducting system of heart
fig. 20-12a
prepotential
cannot maintain steady resting potential
gradually drift toward threshold
SA node
80-100 bpm
AV node
40-60 bpm
fig. 20-12b
because SA node is faster…
…it controls the heart rate
(pacemaker)
but heart rate is normally slower
than 80-100 bpm
(parasympathetics)
if SA node is damaged, heart can still
continue to beat, but at a slower rate
if heartbeat is slower than normal…
… bradycardia
if heartbeat is faster than normal…
… tachycardia
impulse conduction
fig. 20-13
impulse conduction
SA node
atria get signal - contract
signal to AV Node
AV node sends signal
to ventricles (time delay)
ventricles contract
after atria are done
damage to any part of conducting
system may result in abnormalities
(EKG)
ECG’s
EKG’s
electrocardiagram
recording of the electrical activity of the
heart (from the surface of the body)
fig 20-14
ECG’s
different components:
P wave
depolarization of the atria
QRS complex
depolarization of the ventricles
bigger
stronger signal
T wave
repolarization of the ventricles
ECG’s
fig 20-14 EKG
ECG’s
to analyze:
size of voltage changes
duration of changes
timing of changes
intervals
ECG’s
fig 20-14 EKG
ECG’s
intervals:
P-R interval
from start of atrial depolarization
to start of QRS complex
time for signal to get from atrium to
ventricles
if longer than 200 msec can mean
damage to conducting system
ECG’s
intervals:
Q-T interval
time for ventricular depolarization
and repolarization
(ventricular systole)
if lengthened, may indicate, [ion]
disturbances, medications,
conducting problems, ischemia, or
myocardial damage.
ECG’s
intervals:
T-P interval
from end of ventricular repolarization
to start of next atrial depolarization
the time the “heart” is in diastole
the “isoelectric line”
fig 20-14 EKG
T-P
interval
ECG’s
intervals:
abnormalities cardiac electrical activity
= cardiac arrhythmias
some are not dangerous
others indicate damage to heart
100 keys (pg. 688)
“The heart rate is normally established by cells of
the SA node, but that rate can be modified by
autonomic activity, hormones, and other factors.
From the SA node the stimulus is conducted to
the AV node, the AV bundle, the bundle
branches, and Purkinjie fibers before reaching
the ventricular muscle cells. The electrical
events associated with the heartbeat can be
monitored in an electrocardiagram (ECG).”
Electrical activity of the heart cells
99 % of heart is contractile cells
similar to skeletal muscle
AP leads to Ca2+ around myofibrils
Ca2+ bind to troponin on thin filaments
initiates contraction (cross-bridges)
but there are differences…
nature of AP
location of Ca2+ storage
duration of contraction
Electrical activity of the heart cells
The action potential
resting potential of heart cells
~ -90mV
threshold is reached near
intercalated discs
signal is AP in an adjacent cell
(gap junctions)
Electrical activity of the heart cells
The action potential
review skeletal muscle
fig. 20-15
Electrical activity of the heart cells
The action potential
once threshold is reached the action
potential proceeds in three steps.
Electrical activity of the heart cells
The action potential - step 1
rapid depolarization
(like skeletal muscle)
Na+ into cell
through voltage-gated channels
(fast channels)
Electrical activity of the heart cells
The action potential - step 2
the plateau
Na+ channels close
Ca2+ channels open for a “long” time
(slow calcium channels)
Ca2+ in balances Na+ pumped out
Electrical activity of the heart cells
The action potential - step 3
repolarization
Ca2+ channels begin closing
slow K+ channels begin opening
K+ rushes out restoring resting pot.
Electrical activity of the heart cells
The action potential - step 3
repolarization
Na+ channels are still inactive
cell will not respond to stimulus
= refractory period
fig. 20-15a
Electrical activity of the heart cells
The role of calcium
extracellular Ca2+ enters cells
during the plateau phase (20%)
Ca2+ entering triggers release of
Ca2+ from sarcoplasmic reticulum
... heart is highly sensitive to
changes in [Ca2+] of the ECF
Electrical activity of the heart cells
The role of calcium
in skeletal muscle, refractory period
ended before peak tension developed…
…summation was possible
…tetanus.
in cardiac muscle refractory period lasts
until relaxation has begun…
…no summation
…no tetanus.
Clinical note:
Heart attacks
blockage of coronary vessels
myocardium without blood supply…
…cells die
(infarction)
myocardial infarction (MI) = heart attack
Clinical note:
Heart attacks
blockage of coronary vessels
due to:
CAD (coronary artery disease)
(plaque in vessel wall)
blocked by clot (thrombosis)
Clinical note:
Heart attacks
blockage of coronary vessels
as O2 levels fall, cardiac cells will:
accumulate anaerobic enzymes
die and release enzymes
LDH
SGOT
CPK
CK-MB
lactose dehydrogenase
serum glutamic oxaloacetic transaminase
creatine phosphokinase
cardiac muscle creatine phosphokinase
to here 3/26
lec # 31
Clinical note:
Heart attacks
anticoagulants (aspirin)
clot-dissolving enzymes
quick treatment will help reduce damage
due to blockage
Clinical note:
Heart attacks
risk factors:
smoking
high blood pressure
high blood cholesterol
high [LDL]
diabetes
male
severe emotional stress
obesity
genetic predisposition
sedentary lifestyle
any 2
more than
doubles
your risk
of MI
The cardiac cycle
contraction
(systole)
relax
(diastole)
fluid (blood) moves
always moves from higher pressure…
…toward lower pressure
fig. 20-16
The cardiac cycle
atrial systole
atrial diastole
together
ventricular systole
ventricular diastole
generic heart rate 75 bpm
fig. 20-17
The cardiac cycle
atrial systole (100 msec)
1+2
blood in atria is pushed through AV
valves into ventricles
(follows path of least resistance)
“tops off” the ventricles
blood in ventricles is called EDV
(end diastolic volume)
3…
end of atrial systole
ventricular diastole begins
The cardiac cycle
ventricular systole (270 msec)
…3
pressure start to rise in ventricle
when it is greater than pressure in
atria, the AV valves will close
(chordae tendineae and papillary m.)
“lubb”
4
pressure continues to build until it can
force open the semilunar valves
The cardiac cycle
ventricular systole (270 msec)
4
up until now, ventricles have been
contracting but no blood has
flowed:
isovolumetric contraction
ventricular volume has not changed
but the pressure has increased
The cardiac cycle
ventricular systole (270 msec)
when pressure in ventricle is
greater than pressure in the
arteries, the semilunar valves will
open
5
ventricular ejection
stroke volume
some blood left behind
end systolic volume (ESV)
The cardiac cycle
ventricular systole (270 msec)
6
as pressure drops below that of
arteries, the semilunar valves will
close again
“Dupp”
The cardiac cycle
ventricular diasatole (430 msec)
7
semilunar valves are shut
AV valves are shut too (temporarily)
isovolumetric relaxation
8
when pressure gets below atrial
pressure, AV valves will open
and ventricle will begin to fill
passively
fig. 20-17
Heart sounds
auscultation
stethoscope
lubb
lubb
DUPP
DUPP
Heart sounds
lubb
closing of the AV valves
as ventricular contraction begins
Heart sounds
DUPP
closing of the semilunar valves
as ventricular relaxation begins
Heart dynamics
cardiac output
heart rate
stroke volume
variation &
adjustments
Heart dynamics
EDV
definitions
end diastolic volume
ventricle is full
beginning to contract
ESV
end systolic volume
ventricle is done contracting
(a little blood left inside)
Stroke volume
SV = EDV - ESV
Heart dynamics
definitions
cardiac output (CO)
CO = HR (heart rate) x SV
how much blood the heart
pumps in a minute
both the SV and the HR can vary
Heart dynamics
both the SV and the HR can vary
fig. 20-20
Heart dynamics
variation in HR
autonomics
dual innervation to SA node
Heart dynamics
HR
parasympathetics
releases ACh
opens K+ channels
lowers the resting potential
(hyperpolarize cell)
slows heart rate
controlled by cardioinhibitory centers in
the medulla oblongatat
Heart dynamics
HR
parasympathetics
controlled by cardioinhibitory centers in
the medulla oblongata
reflexes
hypothalamus
Normal:
Parasympathetics:
fig 20-22
Heart dynamics
HR
sympathetics
releases NE
binds to beta-1 receptors
opens Na+/Ca2+ channels
depolarize cell
speeds up heart rate
Heart dynamics
HR
sympathetics
controlled by cardioacceleratory centers
in the medulla oblongata
reflexes
hypothalamus
Normal:
Sympathetics:
fig 20-22
Heart dynamics
HR
atrial (Bainbridge) reflex
increased venous return
stretches atria
stimulates stretch receptors
stimulates sympathetics
increase HR
(and CO)
Heart dynamics
HR
hormones
E, NE, thyoid hormone
affect SA node
speed up HR
to here 3/30/07
lec# 33
Heart dynamics
stroke volume (SV)
remember
SV = EDV - ESV
Heart dynamics
SV
EDV
the amount of blood in the ventricle at
the end of its diastolic phase, just
before contraction begins.
Heart dynamics
SV
EDV
affected by the filling time
&
venous return
preload
Heart dynamics
SV
EDV
preload
the degree of stretching of the
ventricle during diastole
preload is proportional to EDV
preload
affects heart muscles ability to
generate tension
Heart dynamics
EDV
preload
SV
Heart dynamics
SV
EDV
preload
“more in = more out”
Frank-Starling principle
fig. 20-23
Heart dynamics
ESV
preload
contractility
afterload
SV
Heart dynamics
SV
ESV
contractility
amount of force generated with
a contraction
increase
+ inotropic action
decrease
- inotropic action
Heart dynamics
SV
ESV
contractility
factors that influence:
ANS
hormones
Heart dynamics
SV
sympathetic NS
NE, E
ESV
+ inotropic effect
contractility
ANS
parasympathetic NS
ACh
- inotropic effect
fig. 20-23
Heart dynamics
SV
NE, E, glucagon,
thyroid hormones
ESV
contractility
hormones
(and drugs)
dopamine,
dobutamine
isoproterenol
digitalis
+ inotropic effect
(hypertension)
Heart dynamics
SV
propanolol
timolol
etc.,
(beta-blockers)
ESV
contractility
hormones
(and drugs)
verapamil
nifedipine
(Ca2+ blocker)
- inotropic effect
fig. 20-23
Heart dynamics
SV
ESV
preload
contractility
afterload
the amount of tension
needed to open semilunar
valves and eject blood
Heart dynamics
SV
ESV
afterload
the amount of tension
needed to open semilunar
valves and eject blood
greater afterload
longer isovolumetric contraction
less ejected, larger ESV
Heart dynamics
SV
ESV
afterload
restrict blood flow
inc. afterload
constrict peripheral vessels
circulatory blockage
fig. 20-23
Summary
Heart rate
hormones
venous return
EDV
filling time
venous return
ESV
preload
contractility
afterload
SV = EDV-ESV
100 keys (pg. 703)
“Cardiac output is the amount of blood
pumped by the left ventricle each minute.
It is adjusted on a moment-to-moment
basis by the ANS, and in response to
circulating hormones, changes in blood
volume, and alternation in venous return.
Most healthy people can increase
cardiac output by 300-500 percent.”